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Studies in Carbohydrate Metabolism Following Guanidine Deglycogenation

Fritz Bischoff and M. Louisa Long

(From The Chemical Laboratory of the Potter Metabolic Clinic, Santa Barbara Cottage Hospital, Santa Barbara)

1. —By means of the diguanidino-polymethylenes it is possible to deplete the glycogen reserves of the liver and destroy the power of this organ to store glycogen, without destroying the power of the muscles to utilize glucose either by its disappearance or storage as glycogen. It is also possible to deplete the glycogen reserves and prevent the storing of glycogen at a hyperglycemic level for both liver and muscle, without destroying the power to utilize glucose.
2. —Insulin increases the utilization of glucose at normal or hyperglycemic levels in guanidine deglycogenated rabbits with or without storing glycogen.
3. —Adrenalin is able to decrease the utilization of injected glucose in animals in which the liver has been depleted of glycogen and has lost the power of storing glycogen through guanidine derivatives, showing that normal adrenalin hyperglycemia is not entirely due to an increased output of glucose by the liver.
4. —Adrenalin increases the blood lactic acid and insulin is without effect upon the blood lactic acid of rabbits suffering guanidine deglycogenation.
5. —Adrenalin increases the blood lactic acid in rabbits whose liver and muscle glycogen reserves have been depleted (less than .01 per cent) by guanidine derivatives.


Manuscript received 17 February 1930.





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